Gelmers H J
Am J Cardiol. 1987 Jan 30;59(3):173B-176B. doi: 10.1016/0002-9149(87)90098-1.
Current research suggests that cerebral ischemia induces a cascade of pathophysiologic reactions. A massive influx of calcium into the neuron constitutes the "final common pathway," resulting in catabolism and cell necrosis due to calcium overload. Treatment with calcium antagonists may offer a means of arresting and possibly preventing the destruction of cerebral tissue in patients with stroke. One such drug, nimodipine, selectively inhibits spasm of isolated cerebral arteries induced by either depolarization or receptor stimulation. In vivo experiments have shown that nimodipine prevents the postischemic impairment of cerebral blood flow that may be a major contributor to neuronal damage. After encouraging although not conclusive results of a single-blind pilot study, a double-blind, placebo-controlled, multicenter clinical investigation of nimodipine was undertaken. Some benefit was strongly suggested in patients with acute ischemic stroke who were treated with 120 mg of nimodipine, begun within 24 hours after the onset of the event, combined with "standard" treatment (i.e., hemodilution using low molecular dextran). Calcium antagonists such as nimodipine may be useful in the treatment of stroke due to acute cerebral ischemia.
目前的研究表明，脑缺血会引发一系列病理生理反应。大量钙离子流入神经元构成了“最终共同通路”，由于钙超载导致分解代谢和细胞坏死。使用钙拮抗剂进行治疗可能为阻止并有可能预防中风患者脑组织破坏提供一种方法。一种这样的药物，尼莫地平，可选择性抑制由去极化或受体刺激诱导的离体脑动脉痉挛。体内实验表明，尼莫地平可预防缺血后脑血流受损，而这可能是神经元损伤的主要原因。在一项单盲试点研究取得虽不确凿但令人鼓舞的结果后，开展了一项关于尼莫地平的双盲、安慰剂对照、多中心临床研究。强烈提示，在急性缺血性中风患者中，在事件发生后24小时内开始使用120毫克尼莫地平并联合“标准”治疗（即使用低分子右旋糖酐进行血液稀释）是有益的。像尼莫地平这样的钙拮抗剂可能对治疗急性脑缺血所致中风有用。
